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Query: UNIPROT:P43026 (
lipopolysaccharide
)
62,215
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Lipopolysaccharide-induced necrosis of grafted tumors was potentiated by several hydrophilic and lipophilic muramyl dipeptide (MDP) derivatives administered a few hours prior to small amounts of
lipopolysaccharide
(
LPS
) in spite of low titers of induced circulating tumor necrosis factor (TNF). However, pretreatment with MDP derivatives did increase the level of TNF in the blood of mice challenged by a greater dose of
LPS
. The TNF amount in 2 h postendotoxin mouse serum reached a peak when the glycopeptide had been given 6 h before the challenge, being approximately 100-fold above that obtained in unprimed mice. The cytotoxic activity in mouse serum was inhibited by rabbit antibodies raised against recombinant mouse TNF. Although there exists a toxic synergism between
BCG
or MDP and endotoxin, the effect of certain MDP derivatives was not related to an increased susceptibility to the toxicity of
LPS
.
...
PMID:Priming effect of muramyl peptides for induction by lipopolysaccharide of tumor necrosis factor production in mice. 230 50
A fraction extracted from
BCG
and designated MY-1, which was composed of 70.0% DNA and 28.0% RNA, was previously reported to possess strong antitumor activities against various syngeneic mouse and guinea pig tumors. An intraperitoneal injection of MY-1 (100 micrograms) 1 day before rendered mouse peritoneal cells cytotoxic to YAC-1 cells. The effector cells were nonadherent to plastic dishes, and the activity was destroyed by treatment with anti-asialo GM1 antiserum plus complement or carrageenan in vitro, but not with carbonyl-iron or anti-Thy 1.2, suggesting that the cells are natural killer (NK) cells. In vivo augmentation of NK activity was dependent on MY-1 dose, and reached the peak 1 day after MY-1 injection. Since NK activity in
lipopolysaccharide
(
LPS
)-nonresponder mice could be augmented by MY-1, the possibility that
LPS
contaminated the MY-1-augmented NK was excluded. MY-1 digested preliminarily with DNase lost its NK-inducing activity, suggesting that the DNA entity of MY-1 was essential for the activity. When mice were pretreated with anti-asialo GM1 or carrageenan, MY-1 could not render the peritoneal cells cytotoxic. Antitumor activities of MY-1 were also abolished if the animals were pretreated with anti-asialo GM1 antiserum or carrageenan, suggesting that the activities can be ascribed mainly to activated NK cells.
...
PMID:In vivo augmentation of natural killer cell activity with a deoxyribonucleic acid fraction of BCG. 242 98
SDS-PAGE analysis of plasma samples from mice injected with high, but nontoxic, concentrations of indomethacin led to the detection of elevated levels of a 125,000 dalton protein. The appearance of this protein was rapid, occurring within 24 hrs after a single injection of the drug. Treatment of mice with similar concentrations of sulindac and derivatives, the indomethacin analogs MK-410 and MK-555, or high doses (1 mg/day) of aspirin, did not induce the appearance of this protein. However, the appearance of this protein was rapidly induced by inflammatory agents such as turpentine or bacterial
lipopolysaccharide
. In addition, the protein was induced by RES stimulating agents such as C. parvum and
BCG
but it was not induced in tumor-bearing animals with activated RE systems. Administration of [3H]-leucine to animals treated with indomethacin, turpentine or
lipopolysaccharide
revealed the accelerated synthesis of primarily the 125 kilodalton protein but also the synthesis of several other plasma proteins as well. These results indicate that treatment of mice with indomethacin uniquely induces changes in plasma proteins with the characteristics of an acute phase response. This ability of indomethacin may reside in its ability to activate murine macrophages.
...
PMID:Treatment of mice with indomethacin leads to the appearance of a 125,000 dalton plasma protein with the characteristics of an acute phase reactant. 244 92
For the purpose of inducing the antitumor effect in the portal vein, the intrasplenic serial biological response modifier (BRM) administration was performed by using our original subcutaneously-imbedded pediculated spleen in the rats. In a view point of endogenous tumor necrosis factor (TNF) production,
lipopolysaccharide
,
BCG
and OK-432 were chosen and injected into the spleen frequently. The study of the portal blood serum revealed that intrasplenic (i.s.) BRM administration group gained higher TNF and interferon (IFN) activity than control group. On the other hand, the study of the mononuclear cells in the portal vein and splenocyte after i.s. BRM administration showed higher cytotoxic activity against YAC-1 cells than control group significantly. Compared with intravenous and intraperitoneal administration groups, i.s. group showed more effective antitumor effects in the portal vein significantly. The experimental liver metastases by intraportal transplantation of AH60C could be cured with i.s. BRM administration, which could increase % survival significantly. According to the result of this study, it is prospective that i.s. serial BRM administration could be new process for suppression of transportal hepatic metastases.
...
PMID:[Induction of endogenous antitumor activities in the portal vein by using a subcutaneously-imbedded pediculated spleen in the rat; experimental study of adjuvant immunotherapy in liver metastases]. 246 67
Serum from Mycobacterium bovis
BCG
-infected mice that had been challenged with
lipopolysaccharide
(
LPS
) exhibited a marked ability to induce gamma interferon (IFN-gamma) in cultures of spleen cells of normal mice in the presence of interleukin-2 (IL-2). The inducing activity became detectable in the circulatory system about 90 min after
LPS
challenge, disappeared at around 5 h, and was observable upon 640x dilution of the serum. Addition of monoclonal anti-IL-2 receptor antibody to the culture inhibited the induction by the serum. The activity induced high levels of IFN-gamma even in nylon wool-nonadherent cells, while concanavalin A failed to do so. Serum from uninfected mice challenged with
LPS
contained no such activity. The molecular weight of the active substance, estimated by gel filtration, was about 70,000. There were pronounced differences among mouse strains in the activities of the sera prepared, which paralleled the amounts of IFN-gamma produced in vivo. However, the levels of IFN-gamma produced in whole spleen cells and in nylon wool-nonadherent cells from mice of various strains were the same when stimulated with competent serum. These results indicate the existence of an unidentified factor that induces IFN-gamma in cooperation with IL-2 in macrophage-depleted splenocytes. They also suggest that IFN-gamma production in vivo is not genetically controlled at the lymphocyte level but, rather, at the level of synthesis of the unknown factor.
...
PMID:Endotoxin-induced serum factor that stimulates gamma interferon production. 249 65
The production of interferon-alpha/beta (INF-alpha/beta) and interferon gamma (IFN-gamma) in NOD and ICR mice was studied in vitro and in vivo. The in vitro IFN-alpha/beta production in the spleen cells of NOD mice, which were stimulated with either Newcastle disease virus (NDV), Sendai virus, poly(I:C) or
lipopolysaccharide
(
LPS
), was very similar to the IFN-alpha/beta production in the spleen cells of ICR mice. Contrastingly, the in vitro IFN-gamma production in the spleen cells of NOD mice, which were stimulated with either concanavalin A (Con A), phytohemagglutinin (PHA) or pokeweed mitogen (PWM), was greater than the IFN-gamma production in spleen cells of ICR mice. The in vivo IFN-alpha/beta production in NOD mice induced by NDV was also very similar to that in ICR mice, whereas the in vivo IFN-gamma production in the
BCG
-sensitized NOD mice, which was induced by purified protein derivative (PPD), was greater than that in the ICR mice. These results may indicate that NOD mice have abnormalities on the IFN-gamma production.
...
PMID:In vitro and in vivo interferon production in NOD mice. 251 17
Macrophages and hepatocytes from normal and
BCG
-primed mice have been spin-labelled in their membranes with 5- and 16-doxyl stearic acid. Incubation of spin-labelled cells from
BCG
-primed animals with
lipopolysaccharide
from E. coli 0111.B4 produced a detectable and transient disturbance in the cell membranes as reflected by an increase in the order parameter measured from the electron spin resonance spectra of 5-doxyl-stearate. This membrane disturbance was maximal at 3-4 hours of incubation and was only detected with cells from mice primed with
BCG
. Spectra obtained from the 16-doxyl-stearate-labelled cells showed no change in order parameter on incubation with
lipopolysaccharide
.
...
PMID:Effects of E. coli 0111.B4 lipopolysaccharide on spin-labelled murine macrophage and hepatocyte membranes. 255 85
BCG
-elicited mouse peritoneal macrophages were separated into three subpopulations by counterflow centrifugal elutriation. The three subpopulations were characterized on the basis of the level of a protein cross-linking enzyme, tissue transglutaminase. Subpopulation-3 consisted of large cells (greater than 95% esterase positive and greater than 90% viable) and had at least a fivefold higher transglutaminase activity (35 +/- 6 nmol/hr/mg) as compared to macrophages in subpopulation-1 (6 +/- 2 nmol/hr/mg) and at least a threefold higher enzyme activity as compared to subpopulation-2 (11 +/- 2 nmol/hr/mg). Subpopulation-3 also showed sevenfold higher phagocytosis of IgG-coated sheep red blood cells. The three subpopulations showed no difference in their ability to kill Listeria monocytogenes as determined by [3H]-thymidine release. Subpopulations-2 and -3 caused 90% inhibition of murine adenocarcinoma (EMT-6) tumor cell growth in the presence or absence of
lipopolysaccharide
. Subpopulation-1 had a poor ability to inhibit EMT-6 cell growth (29 +/- 12%). However, in the presence of
lipopolysaccharide
, this activity increased by at least threefold (92 +/- 7%). The three subpopulations showed no significant difference in their cytolytic activity against murine mastocytoma (P815) target cells in the presence or absence of
lipopolysaccharide
. These results suggest that tissue transglutaminase may have no significant role in bactericidal, tumoricidal, or tumoristatic function of macrophages; however, it might have some role in promoting the Fc-receptor-mediated phagocytic function of the macrophages.
...
PMID:Transglutaminase levels and immunologic functions of BCG-elicited mouse peritoneal macrophages isolated by centrifugal elutriation. 256 58
The comparative abilities of various reagents to prime rabbit alveolar macrophages (AM) to produce reactive oxygen intermediates (ROI) in a chemiluminescent (CL) assay were investigated. It was noted that AM from normal rabbits cultured in a serum-free medium for 18 hr exhibited a "spontaneous" priming response following a challenge with phorbol myristate acetate (PMA); however, "spontaneous" priming was not evident when the AM were cultured for only 3 hr. It was further established that pretreatment of normal AM for 3 or 18 hr with MIF/MAF preparations (serum-free), fetal bovine serum (FBS), or bovine serum albumin (BSA) exhibited marked increases in their CL responses following challenge with PMA. When FBS was used in the culture medium, the priming activity of MIF/MAF was masked because of the high CL responses of controls due to the priming effects of FBS. BSA at concentrations approximately equivalent to the amount in FBS also displayed marked priming activity. Bacterial products (
lipopolysaccharide
and muramyl dipeptide), latex particles, rabbit IgG, PMA, and opsonized as well as nonopsonized zymosan and bacteria (
BCG
and Staphylococcus epidermidis) were inactive as priming agents. In comparison, AM from
BCG
-immune rabbits that were primed in vivo yielded a very large CL response when challenged with PMA. Opsonized zymosan and bacteria produced twofold increases in the CL responses in
BCG
-immune AM compared to nonopsonized preparations. The marked priming effect of serum on AM cultured for even a short period (3 hr) indicates that normal AM undergo marked changes in culture that complicate the interpretation of AM function when AM are cultured in vitro in media containing serum.
...
PMID:Oxidative responses of rabbit alveolar macrophages: comparative priming activities of MIF/MAF, sera, and serum components. 264 82
The murine macrophage-like cell line J774.16 and peritoneal exudate cells elicited with thioglycollate or starch contain a major calmodulin (CaM)-binding protein (CaMBP) which is absent in trifluoperazine-resistant variants of J774, resident peritoneal macrophages and peritoneal macrophages elicited with concanavalin A,
lipopolysaccharide
, proteose peptone, or
Bacillus Calmette-Guerin
. Resident murine peritoneal cells maintained in tissue culture for 3 days begin to accumulate this protein, as do human peripheral blood monocytes after 7 days of culture. A specific competitive displacement radioimmunoassay was developed with the use of a rabbit antiserum raised to the partially purified CaM-binding protein and [125I]CaM covalently cross-linked to the principal CaM-binding protein in the preparation. The radioimmunoassay confirmed the unique cellular distribution of this protein, suggesting that it may be a marker for certain stages of macrophage differentiation. Monoclonal antibodies were prepared, and one of these was used to further purify the protein by immunoaffinity chromatography. A protein of Mr 50,000 to 60,000 was isolated. The protein could be selectively adsorbed to wheat germ agglutinin agarose and subsequently eluted with N-acetyl glucosamine. This property, plus the sensitivity of the protein to endoglycosidase F, led to the conclusion that it is a glycoprotein. The cellular distribution, subcellular localization, and evidence for glycosylation suggest that this protein may be a macrophage-specific receptor with a high affinity for Ca2+-CaM.
...
PMID:Purification and distribution of a novel macrophage-specific calmodulin-binding glycoprotein. 298 Oct 93
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